Dose‐dependent effects of nicotine on proliferation and differentiation of human bone marrow stromal cells and the antagonistic action of vitamin C

A range of biological and molecular effects caused by nicotine are considered to effect bone metabolism. Vitamin C functions as a biological antioxidant. This study was to evaluate the in vitro effects of nicotine on human bone marrow stromal cells and whether Vitamin C supplementation show the antagonism action to high concentration nicotine. We used CCK‐8, alkaline phosphatase (ALP) activity assay, Von Kossa staining, real‐time polymerase chain reaction and Western Blot to evaluate the proliferation and osteogenic differentiation. The results indicated that the proliferation of BMSCs increased at the concentration of 50, 100 ng/ml, got inhibited at 1,000 ng/ml. When Vitamin C was added, the OD for proliferation increased. For ALP staining, we found that BMSCs treated with 50 and 100 ng/ml nicotine showed a higher activity compared with the control, and decreased at the 1,000 ng/ml. Bone morphogenetic protein‐2 (BMP‐2) expression and the calcium depositions decreased at 100 and 1,000 ng/ml nicotine, while the addition of Vitamin C reversed the down regulation. By real‐time PCR, we detected that the mRNA expression of collagen type I (COL‐I) and ALP were also increased in 50 and 100 ng/ml nicotine groups (P < 0.05), while reduced at 1,000 ng/ml (P < 0.05). When it came to osteocalcin (OCN), the changes were similar. Taken all together, it is found that nicotine has a two‐phase effect on human BMSCs, showing that low level of nicotine could promote the proliferation and osteogenic differentiation while the high level display the opposite effect. Vitamin C could antagonize the inhibitory effect of higher concentration of nicotine partly. J. Cell. Biochem. 114: 1720–1728, 2013. © 2013 Wiley Periodicals, Inc.     

重金属对海洋桡足类的影响研究进展

桡足类是海洋浮游动物种群的主要组成部分和重要的初级消费者,重金属污染对其影响可通过食物链传递到其他海洋生物甚至人类。综述了近20 a来重金属对桡足类影响的研究进展,包括重金属对桡足类的毒性和生理效应,重金属在桡足类体内蓄积及桡足类体内重金属的食物链(网)传递。并指出今后的研究重点:桡足类体内致毒重金属的存在形式,重金属食物暴露对桡足类生理生化影响机理,以及重金属对桡足类生活史的影响。     

食细菌线虫Caenorhabditis elegans的取食偏好性

通过设置平板培养试验,以模式种线虫 Caenorhabditis elegans 为材料,观察了食细菌线虫的取食行为。结果表明：C. elegans 在取食细菌时对原位土壤中分离的一种Pseudomonas sp细菌存在最大的取食偏好性。这种取食偏好性表现在大部分C. elegans 在24 h内都直接朝Pseudomonas sp迁移,说明C. elegans能通过某种机制识别Pseudomonas sp。距离迁移试验及C. elegans迁移率表明它可能是通过辨别细菌所发出的气味识别它喜欢的食物。C. elegans的繁殖率跟其取食的偏好性是相关的,在迁移率较高的细菌培养基中线虫表现出更高的繁殖率。结果还表明：相对于G+细菌而言, C. elegans 偏好取食G-细菌。为进一步了解土壤生态系统中食细菌线虫与细菌群落结构间相互关系提供了帮助。     

LncRNA PCAT‐1 promotes tumour growth and chemoresistance of oesophageal cancer to cisplatin

Oesophageal cancer (OC) is one of the most fatal malignancies in the world, and chemoresistance restricts the therapeutic outcome of OC. Long noncoding RNA (lncRNA) was reported to play roles in multiple cancer types. Yet, the function of lncRNA in chemoresistance of OC has not been reported. A lncRNA gene, PCAT‐1, showed higher expression in OC tissues, especially higher in secondary OC compared with normal mucosa tissues. Overexpression of PCAT‐1 increased the proliferation rate and growth of OC cells. Inhibition of PCAT‐1 decreased proliferation and growth of OC cells, and increased cisplatin chemosensitivity. In a mouse OC xenograft model, PCAT‐1 inhibition repressed OC growth in vivo. Therefore, PCAT‐1 may potentially serve as a therapeutic target for treating OC. PCAT‐1 promotes development of OC and represses the chemoresistance of OC to cisplatin, and silencing of PCAT‐1 may be a therapeutic strategy for treating OC.